When the bone marrow transplant failed to treat my leukaemia, it was like: this is it, there’s nothing else now. The doctors were telling my parents it was a matter of weeks. Not years, not months, but weeks.

I’d just turned 13, and I was thinking: “Oh my gosh, this is my last birthday. I’m never gonna grow up and have a family and do all the things that normal people are completely used to, like those normal, everyday things.”

But then we heard about the trial and went down to Great Ormond Street Hospital in London. It was like sci-fi. They were like: “Oh, we’re gonna put some CAR Ts in, and they’re gonna multiply and multiply some more, and go around and fight and kill your all your cancer cells.”

It all started after Easter in 2021. When I went back to school after the coronavirus lockdown ended, I was really tired. I found it hard to walk home from school; I was falling asleep during breaks and lunches. Eventually, I was too sick to go to school.

Really early one morning, my dad noticed my breathing didn’t sound good, and we ended up in A&E. When they put the monitor on me, they started shouting for help. I was in intensive care with double pneumonia for days, and when I woke up, I found out I’d already been put on chemotherapy for leukaemia – that’s when the immune cells in your blood turn cancerous.

Mum and Dad say it took the doctors a few days to work out what was wrong. That might be because I had T-cell leukaemia, which is less common than B-cell leukaemia.

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Then it all moved really quickly. I had a month of chemo at Leicester Royal Infirmary. It wasn’t working, so I was put on more intense chemo, but that didn’t work either. So at the end of October, I went to Sheffield Children’s Hospital for a bone marrow transplant. The idea is, you kill off the blood stem cells, including the cancerous ones, and then you replace them with the transplant.

I was there for five and a half weeks, and I was like, I’m not spending Christmas in hospital, no. And I did get home for Christmas, but afterwards I got a fever and had to go back to Sheffield. That’s when we found out that the transplant hadn’t worked.

There was nothing else the doctors could do. For me, I don’t think it really sunk in at the time. But for Mum and Dad, it was hard. Mum says nothing was harder than not having hope.

She and Dad started looking everywhere, trying to find out if there was anything at all that could work, if we could go to other countries. They were looking at remortgaging the house and things. And they kept on hearing about CAR Ts – that’s when you change T-cells so they kill cancerous cells – and how they can work when bone marrow transplants fail. But they soon realised it only works for B-cell leukaemia, because if you make T-cells attack T-cells, they just kill each other.

Then my consultant from Sheffield heard about a trial Professor was organising. He was using CRISPR base editing to change the CAR T-cells so they don’t look like T cells anymore and so don’t kill each other. And my consultant was like, my patient might be a really good fit. That’s when we went down to Great Ormond Street to meet Professor Waseem and Doctor , who ran the trial.

Mum and Dad weren’t sure about me doing the trial. They were worried it wouldn’t work and I’d spent my last weeks in hospital in pain, when we could do stuff like going to Disneyland instead. But they let me make the decision.

I was like, I’m doing it. If it’s not gonna help me, it’s gonna help someone else. I was 13 then, I hadn’t really had a chance to do anything, I wasn’t leaving behind anything, I’d had no impact. So it was a way for me to take control of something that I hadn’t been in control of for such a long time, and to try to make a difference for someone else, even if it didn’t work for me.

I had two weeks of conditioning in hospital before I had the CAR T-cells. We had some camera crews film it; it was really amazing. A week later, Dr Chiesa told us they’d multiplied. It was the first sign it was working.

Everybody at Great Ormond Street was so great. I made a friend even though we didn’t meet each other for two months, we just texted, and got the nurses and the play specialists to put stuff on each other’s windows. And I had another friend who was next door to me, but unfortunately she wasn’t able to have a bone marrow transplant, so she passed away.

After four weeks, they tested my bone marrow, and there was nothing there. There were no blood cells to detect. Two weeks later, there was still nothing there, so we went ahead and did my second bone marrow transplant, to replace the blood stem cells.

The hardest part was going home. In the hospital, there was almost always someone around that you could talk to. But then when I went home, I wasn’t allowed out of the house in case I caught something, and I wasn’t allowed to see any of my friends. Mum started going back to work, so it was just me and my dog Holly for almost a year.

I’m still in remission, but not everything is resolved. My thyroid is underactive, but that’s because of all the chemo, not because of the CAR Ts. This is why it’s so important to keep pushing it, so maybe someday people won’t have to have this intensive chemo and can go straight on to have CAR Ts.

I turned 17 in January. I’m doing my A-levels and learning to drive now, which is a bit scary. I want to get a degree apprenticeship in biomedical science. If I can do half as much for someone as the treatment did for me, it would be amazing.

I also get to go to conferences to talk about my experience. At one of them, we met Professor David Liu, who developed base editing. I actually cried when I met him. The video’s quite embarrassing.

I’m so pleased and privileged to have the opportunity to go and do these things, and talk about why science is so important, and why research is so important. Without it, I wouldn’t be here.

As told to Michael Le Page

A tiny genetic tweak can make pigs completely resistant to classical swine fever, a major problem for farmers around the world. The same gene edit should also make cattle and sheep resistant to related viruses that plague livestock.

The widespread use of gene-edited pigs resistant to classical swine fever would improve animal welfare and increase productivity, which should lead to lower greenhouse gas emissions and lower prices in shops. “It would help towards sustainable livestock production, and with nice healthy, happy pigs,” says at the UK’s Animal and Plant Health Agency.

Classical swine fever is a highly contagious viral disease that causes everything from fevers to diarrhoea and miscarriages, and can kill large numbers of pigs.

Although the disease has been eliminated in many regions, it occasionally re-emerges. Six million pigs were culled to halt an outbreak in the Netherlands in 1997, for instance, while Japan has been struggling to re-eliminate the disease since 2018.

Where the disease is present, vaccines containing live, weakened strains of the virus are used to protect livestock, but this is laborious and expensive. “Vaccination takes a lot of coordination and monitoring,” says at the University of Edinburgh, UK.

Countries that vaccinate cannot export to disease-free regions. And any disruption to vaccination can lead to outbreaks – this happened in the Philippines recently, says Tait-Burkard.

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But the classical swine fever virus has an Achilles heel. A bunch of the virus proteins are made as a single long strand of amino acids that has to be cut into pieces to become functional, and it relies on a pig protein to do the cutting.

Changing a single amino acid in this pig protein, called DNAJC14, can block the cutting. So Tait-Burkard and her colleagues used CRISPR gene editing to create pigs with this tiny change.

The team then sent some of the pigs to a secure facility, where Crooke and her colleagues sprayed live swine viruses into their noses. None developed any signs of infection – no symptoms, antibodies or detectable viruses – whereas normal pigs all fell ill.

“These animals were completely resistant to replication of the virus and remained happy and healthy throughout the study,” says Crooke.

The work was partly funded by a large international breeding company called Genus, which is now considering whether to commercialise the pigs.

Genus has already created gene-edited pigs resistant to another major disease called porcine reproductive and respiratory syndrome. These pigs have now been approved in the US, Brazil and other countries. Genus is awaiting approval in Mexico, Canada and Japan – key export markets for the US – before starting to sell semen to farmers.

Where gene editing is used to make tiny changes that could occur naturally, many countries are regulating it less strictly than conventional genetic engineering. Japan has already approved three gene-edited fish.

England is due to start approving gene-edited plants soon, but has yet to finalise the rules for livestock. These rules will almost certainly require that gene edits don’t affect welfare.

The team hasn’t seen any adverse effects in the pigs that are resistant to classical swine fever, says , a team member at the University of Edinburgh, but further studies will be needed to confirm this.

He also notes that there are no such welfare requirements with conventional breeding. “A level playing field would be lovely,” he says. “There are certainly traditionally bred animals that have lower welfare associated with them.”

Viruses very closely related to classical swine fever cause bovine viral diarrhoea in cattle and border disease in sheep. The cattle and sheep diseases are less deadly, but do still affect welfare and productivity. The Edinburgh team is now investigating whether the change made in pigs will work in cattle and sheep too.